Glioblastomas are deadly cancers characterized by rapid cell proliferation, high invasiveness, and resistance to radio- and chemotherapy (Nakada et al., (2007) Cell. Mol. Life Sci. 64: 458-478). Patients with this aggressive tumor, which accounts for nearly 50% of all adult brain tumors, have a median survival of approximately 15 months (Nagasawa et al., (2012) Neurosurgery Clinics N. Am. 23: 307-322). The standard treatment for glioblastoma involves invasive surgery and radiotherapy, which is often followed by chemotherapy with temolozomide (Hegi et al., (2005) New Eng. J. Med. 352: 997-1003). As the development of novel therapeutic treatments for glioblastoma are desperately needed, it is essential to understand the molecular mechanisms supporting growth and survival of this highly malignant and practically incurable brain tumor.
Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by the lack of estrogen receptor, progesterone receptor, and HER-2. Consequently, TNBC cannot be treated by the available hormone therapies and receptor targeted treatments. MYC, a regulatory gene involved in cell growth, metabolism, differentiation, and apoptosis, is disproportionately overexpressed in many TNBCs, making it a valuable therapeutic target.
MicroRNAs (miRNAs) are non-translated RNA species typically of 19 to 25 nucleotides in length whose function is to mediate post-transcription regulation of gene expression. miRNAs bind to the 3′ untranslated region (3′UTR) of target messenger RNAs (mRNAs), resulting in translation inhibition or degradation of the mRNA transcript and subsequent reduction in protein production.
Clinically, specific miRNAs may serve as a therapeutic target or therapeutic agent depending on their role in human health and disease, a notion that is particularly relevant for the treatment of various cancers. In this regard, intense research is focused on inhibiting an overexpressed miRNA molecule or reintroducing the depleted miRNA molecule, respectively, for the treatment of various cancers. As a therapeutic agent, miRNAs are particularly promising as they are relatively cheap to synthesize, and because as their intrinsic stability confers a longer in vitro activity. In addition, since they are endogenously produced by the cells their expression can be triggered by different agents and/or molecular tools; therefore suggesting their use in combination with other anti-cancer drugs, such as fenofibrate.